Mercury in molar excess of selenium interferes with thyroid hormone function in free-ranging freshwater fish.

Thyroid hormones (THs) are essential for cellular metabolism, somatic growth and development, and reproduction. Mercury (Hg) entering aquatic systems and accumulated as highly toxic methylmercury (MeHg) represents a threat to wildlife and human health. Selenium (Se) is an essential element critical for TH activation and regulation. In organisms, binding of Hg in a Se-Hg complex results in a detoxification of Hg. However, formation of Se-Hg complexes also affects Se bioavailability, disrupting functions of Se-dependent enzymes, such as TH deiodinases, which convert thyroxine (T4) to the physiologically active TH, triiodothyronine (T3). The main aim of the present study was to investigate how tissue Se:Hg molar ratios, tissue levels of Se and Hg, and other potential TH disruptive contaminants (metals and organic chemical compounds) affect plasma TH levels in free-ranging brown trout, Salmo trutta , from Lake Mjøsa (a Se-deprived lake) and Lake Losna (a reference lake), Norway. Among the wide range of potential TH disruptive pollutants investigated, tissue Se:Hg molar ratios in muscle and liver were the most significant predictors of plasma TH levels in the trout. Moreover, lower plasma levels of the biological active hormone, T3, in the Lake Mjøsa trout co-occurred with their low Se:Hg molar ratios. This suggests that Se availability is impaired by Hg and results in altered selenoenzyme activities and loss of optimal control of TH balance in free-ranging freshwater fish.

Selenium moderates mercury toxicity in free-ranging freshwater fish.

Due to the extremely high affinity of selenium (Se) to mercury (Hg), Se sequesters Hg and reduces its biological availability in organisms. However the converse is also true. Hg sequesters Se, causing Hg to inhibit the formation of Se dependent enzymes while supplemental Se supports their continued synthesis. Hence, whether or not toxic effects accompany exposure to Hg depends upon the tissue Se:Hg molar ratio of the organism. The main objective of the present study was to investigate how levels of Hg and Se affected metallothionein (MT) induction in free-ranging brown trout, Salmo trutta, from Lake Mjøsa, Norway (a Se depauperate lake). MT is proposed as a sensitive biomarker of potential detrimental effects induced by metals such as Hg. Emphasis was addressed to elucidate if increased tissue Se:Hg molar ratios and Se levels affected the demands for MT in the trout. The Se:Hg molar ratio followed by tissue Se levels were most successful for assessing the relationship between metal exposure and MT levels in the trout. Thus, Hg in molar excess over Se was a stronger inducer of MT synthesis than tissue Hg levels in the trout, supporting the assumption that Se has a prominent protective effect against Hg toxicity. Measuring Hg in animals may therefore provide an inadequate reflection of the potential health risks to humans and wildlife if the protective effects of Se are not considered.